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Related Concept Videos

Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
Skeleton and Calcium Homeostasis01:21

Skeleton and Calcium Homeostasis

Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Relaxation of Skeletal Muscles01:29

Relaxation of Skeletal Muscles

The period of muscle contraction primarily influences the duration of stimulation at the neuromuscular junction (NMJ), the presence of free calcium ions in the sarcoplasm, and the availability of energy or ATP to support contractions.
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
Enlargement of the Plasma Membrane01:22

Enlargement of the Plasma Membrane

Cell division and enlargement are processes that require precise control. The control ensures that cell division cannot proceed unless the cell has grown to a specific size. A spherical, dividing cell requires an approximately 1.6X increase in its surface area to double its volume. The secretory pathway also has a significant role in cell membrane enlargement. Secretory vesicles that bud off from the Golgi apparatus and later fuse with the plasma membrane during exocytosis are a major source of...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...

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Related Experiment Video

Updated: Jun 5, 2026

Direct Imaging of ER Calcium with Targeted-Esterase Induced Dye Loading (TED)
09:32

Direct Imaging of ER Calcium with Targeted-Esterase Induced Dye Loading (TED)

Published on: May 7, 2013

Refilling Intracellular Calcium Stores.

Changwon Kho1, Ahyoung Lee, Dongtak Jeong

  • 1Cardiovascular Research Center, Mount Sinai School of Medicine, New York, NY10029, USA.

Drug Discovery Today. Disease Mechanisms
|December 21, 2010
PubMed
Summary

Calcium ion regulation by the sarcoplasmic reticulum (SR) is crucial for heart function. This review explores how SR protein changes in heart failure disrupt calcium (Ca2+) balance and impair contraction, highlighting therapeutic targets.

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Related Experiment Videos

Last Updated: Jun 5, 2026

Direct Imaging of ER Calcium with Targeted-Esterase Induced Dye Loading (TED)
09:32

Direct Imaging of ER Calcium with Targeted-Esterase Induced Dye Loading (TED)

Published on: May 7, 2013

Cytosolic Calcium Measurements in Renal Epithelial Cells by Flow Cytometry
10:24

Cytosolic Calcium Measurements in Renal Epithelial Cells by Flow Cytometry

Published on: October 28, 2014

Monitoring ER/SR Calcium Release with the Targeted Ca2+ Sensor CatchER+
12:30

Monitoring ER/SR Calcium Release with the Targeted Ca2+ Sensor CatchER+

Published on: May 19, 2017

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Physiology

Background:

  • Cardiac cells rely on precise calcium ion (Ca2+) regulation for normal contraction.
  • The sarcoplasmic reticulum (SR) is a key organelle managing intracellular Ca2+ movements.
  • Dysregulation of SR proteins contributes to the pathophysiology of heart failure.

Purpose of the Study:

  • To review the role of SR Ca2+ regulators in cardiac disease.
  • To discuss novel therapeutic strategies targeting SR Ca2+ pathways in heart failure.

Main Methods:

  • Literature review of studies on SR Ca2+ handling in cardiac function and disease.
  • Analysis of current research on therapeutic interventions targeting SR proteins.

Main Results:

  • Alterations in SR Ca2+ regulatory proteins are linked to abnormal Ca2+ homeostasis in failing hearts.
  • These disruptions lead to impaired cardiomyocyte contractility.
  • Emerging therapeutic strategies aim to restore normal SR Ca2+ handling.

Conclusions:

  • Targeting SR Ca2+ regulatory proteins offers a promising avenue for treating heart failure.
  • Understanding SR Ca2+ dynamics is critical for developing effective cardiac therapies.